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Basophil‐bound IgE and serum IgE directed against Haemophilus influenzae and Streptococcus pneumoniae in patients with chronic bronchitis during acute exacerbations
Author(s) -
KJÆRGÅRD L. L.,
LARSEN F. O.,
NORN S.,
CLEMENTSEN P.,
SKOV P. STAHL,
PERMIN H.
Publication year - 1996
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1996.tb00687.x
Subject(s) - immunoglobulin e , streptococcus pneumoniae , haemophilus influenzae , immunology , basophil , chronic bronchitis , histamine , microbiology and biotechnology , basophil activation , allergen , medicine , biology , allergy , antibody , antibiotics
The investigation includes 12 patients hospitalized with acute exacerbations of chronic bronchitis (CB) and infected in the lower respiratory tract with Haemophilus influenzae (HI) or Streptococcus pneumoniae (SP). Eight patients were infected with HI, three with SP, and one patient with both species. Basophil‐bound IgE and serum IgE directed against these species were examined using the patients' own bacterial isolates. All patients showed IgE‐mediated histamine release when their peripheral leukocytes were incubated in vitro with the infecting species, indicating basophil‐bound IgE directed against their own bacterium. No IgE‐mediated response was obtained in the control group of 12 healthy individuals. Bacteria‐specific IgE in serum was demonstrated by immunofluorescence assay and further verified by passive sensitization. There was a positive serum titre in seven of nine patients housing HI and in all SP‐infected patients but not in the control group. No synchronism was found between a positive response in the histamine release test and the immunofluorescence assay by parallel testing during the test period. This may be due to a time delay between production of serum IgE and its fixation to the cell surface. The results indicate a potential for a bacteria‐specific IgE‐mediated immune response in CB. Thus, by triggering mediator release, bacteria may be involved in the pathogenesis of exacerbations in CB.